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Biomedical subjects

C Meier

Publications and source records attributed to C Meier.

At least 217 records · Page 12Linked to original sources
PubMed1977

Regeneration of cauda equina fibres after transsection and end-to-end suture. Light and electron microscopic study in the pig.

The regeneration of nerve fibres in pigs was studied three months after transection and end-to-end suture of the dorsal and ventral spinal nerve roots L5 and S1. Although no detailed quantitative analysis was performed, it was clearly evident that regeneration in motor roots is significantly more efficacious than in sensory roots. Probably as a reaction to Wallerian degeneration, an increase of histiocytes, fibroblasts and collagen fibrils, as well as a thickening of the sheaths was observed in the transected and sutured roots. Heterotopic glial bundles were found in the regenerated dorsal roots.

Animals↗
PubMed1977

[Gentamicin neurotoxicity (polyneuropathy--encephalopathy)].

An investigation has been conducted into clinical signs and concomitant ultrastructural alterations in the peripheral nerves of 4 patients who developed polyneuropathy and, in part, encephalopathy following gentamicin therapy. The ultrastructural analysis of the nerve biopsy afforded evidence of an induced lysosomal abnormality comparable to the changes observed in gentamicin nephrotoxicity. As in nephrotoxicity, the neurotoxic effect seems to be reversible.

Aged↗
PubMed1977

[Surface analysis of 2 composite filling materials after various methods of finishing and sealing].

The surface quality of 2 composite filling materials (Adaptic with coarse hard quartz fillers and Cosmic with fine softer glass fillers) was evaluated using profilometry, scanning electron microscopy and light reflectometry after finishing with experimental diamond discs, 3M discs, corundum discs, polishing paste and also after sealing. Plaque formation on standardized surfaces of both composites was photographically recorded in 20 subjects. The sealed surfaces and the surfaces finished by the matrix alone were approximately 10 times less rough than after finishing procedures. Under in vivo conditions they reflected the most light, for both composites. The sealer failed to cover the whole composite surface. The unfinished and sealed surfaces lost their shine 3-7 days after placement in the mouth. Decrease in reflectance was independent of mechanical oral hygiene procedures. There were no significant differences in the roughness produced by the various discs on Adaptic surfaces. Diamond discs with particle size 1-3 micrometer resulted in least surface roughness and were the only instruments not destroying the filler particles of either composite. 3M discs and the rough corundum discs caused significantly more surface roughness of the Cosmic surface. Reflectometry showed that the finishing methods unfavourably affected composite surface smoothness. Among all finishing methods polishing paste produced the highest reflection value on the Cosmic surface. Adaptic surfaces were always associated with more plaque formation than Cosmic surface after all finishing methods.

Composite Resins↗
PubMed1977

[Hepatitis B antigen (HBSAG) in hospitalized children].

Blood samples of 1940 hospitalized children aged 0--18 years were investigated for presence of HBs-Ag by counter-electrophoresis, haemagglutination and radioimmunoassay, HBs-Ag was found in 1.34% of all patients, being distributed evenly amongst boys and girls. The incidence was 1.7% in patients from a large University children's hospital and 0.6% in patients from a group of regional hospitals. Of 26 samples positive by radioimmunoassay, 1 only was found positive by insensitive counter-electrophoresis. In addition to diseases known to be correlated with HBs-antigenaemia in adults, there was an accumulation of inborn deformities as well as perinatal and neurologic disorders in HBs-Ag positive children. Vertical transmission of hepatitis-B virus from pregnant or nursing mothers to their children could not be found. The incidence of HBs-antigenaemia increases little with age, thus infection in early childhood appears probable at least in a part of the cases.

Abnormalities, Multiple↗
PubMed1976

Sequence of morphological alterations in the nervous system of metachromatic leucodystrophy. Light- and electronmicroscopic observations in the central and peripheral nervous system in a prenatally diagnosed foetus of 22 weeks.

Light and electronmicroscopic findings are reported in a case of metachromatic leukodystrophy diagnosed prenatally who died after iatrogenic abortion during the 23th week of gestation. The brain of this foetus was not yet myelinated while the spinal cord showed early, and the peripheral nerves advanced myelination. The onset and the degree of myelination were similar as in a normal foetus of the same age. Ultrastructurally there was evidence of sulphatide storage before the beginning of myelination. During myelination lysosomal storage material, staining metachromatically in acid cresyl violet preparations, appeared in oligodendrocytes and Schwann cells. Besides sulphatide storage material, prominent amounts of neutral lipids were found in oligodendrocytes. Myelin breakdown was encountered very seldom.

Central Nervous System↗
PubMed1976

Some observations on early myelination in the human spinal cord. Light and electron microscope study.

Segments of cervical spinal cord from a 23-week-old human foetus have been examined by light and electron microscopy. Myelinated fibres were found in the dorsal, ventral and peripheral lateral tracts, while the lateral corticospinal tract was completely unmyelinated. Myelin sheaths appeared to be formed by spiral wrapping of elongated mesaxons which originated from the apposition of the plasma membranes of oligodendrocytes. Preparations stained with Sudan red and Sudan black revealed the occurrence of lipid inclusions in the interfascicular glia. The topographical relation and the ultrastructural features of these inclusions are described. The possible significance of the inclusion bodies is discussed.

Axons↗
PubMed1976

Dynamic aspects of peripheral nerve changes in progressive neural muscular atrophy: light- and electronmicroscopic studies of serial nerve biopsies.

Serial nerve biopsies were performed at an early, and at an advanced stage of the disease in 2 patients with progressive neural muscular atrophy. The early biopsy showed a complete loss of the large diameter and thickly myelinated fibres, as well as an expansion of the endoneurial interstitium in both cases. Myelinated and unmyelinated fibres exhibited axonal degeneration in all biopsies occasionally. "Onion bulb" formation, a typical feature of peripheral neuropathy in neural muscular atrophy, was found to be prominent only in the latter biopsies. As regards the formal pathogenesis of hypertrophic neuropathy in neural muscular atrophy, axonal dystrophy and interstitial changes of the endoneurium were regarded as primary phenomena, demyelination and "onion bulb" formation as secondary. A possible causal relation between axonal dystrophy and interstitial changes, observed in these cases, is discussed in the light of the present literature.

Adolescent↗
PubMed1976

Spondyloepiphyseal dysplasia, corneal clouding, normal intelligence and acid beta-galactosidase deficiency.

A 14-year-old girl with a unique type of progressive spondyloepiphyseal dysplasia, corneal clouding, and no evidence of neurological abnormality, was found to have a remarkable deficiency of acid beta-galactosidase activity in cultured skin fibroblasts and in leucocyte preparations. In fibroblasts, ganglioside GM1 beta-galactosidase activity averaged 7% of the normal mean while asialofetuin beta-galactosidase and 4-methylumbe lifery-beta-galactosidase averaged 1.4% and 3.5%, respectively. Activities for all three substrates in leucocytes from both her parents were close to 50% of the normal mean indicating that the patient is homozygous for a mutation (or mutations) affecting GM1 beta-galactosidase.

Adolescent↗
PubMed1976

Chemical compositions of brain and myelin in two patients with multiple sulphatase deficiency (a variant form of metachromatic leukodystrophy).

The lipid composition of the brain, including myelin, was studied in detail in two cases with a variant form of metachromatic leukodystrophy (multiple sulphatase deficiency type). In the white matter, the sulphatide concentration was 3-4 times higher than the normal level in both cases. There was a significant accumulation of cholesterol sulphate in the brain, liver and kidney of both cases. The ganglioside pattern in the grey and white matter was abnormal, with a higher proportion of GM3, GM2 and GD3-gangliosides. Non-lipid hexosamine contents were increased 1.5-2 times in brain, 8-10 times in liver and 2-3 times in kidney. Increased amounts of glucocerobroside, ceramide lactoside and ceramide trihexoside were present in grey and white matter of both cases. Recovery of purified myelin from two patients' brains was much less than from control (1-2% in case 1 and 20-30% in case 2). The lipid composition of myelin was almost normal except for a higher proportion of sulphatide, with a decreased amount of cerebroside. The fatty acid compositions of myelin sulphatide and sphingomyelin were almost normal, while non-hydroxy fatty acids of cerebroside contained less long-chain fatty acids, as characterized by a significant increase of C16:0 and C18:0 fatty acids. The myelin polypeptide pattern by SDS-disc gel electrophoresis showed a relative decrease of basic protein and of proteolipid protein. A possible mechanism of myelin loss in MSD is discussed.

Antigens, CD↗
PubMed1975

[Polyneuropathy in vitamin B 12 and folic acid deficiency. Clinical and histopathological study with electron-microscopy analysis of the sural nerve].

One case each of pernicious anemia and folic acid deficiency with chronic malabsorption with disease of the cord and histologically demonstrated concomitant disease of the peripheral nerve system in the sense of a polyneuropathy are described. The histological findings of nerve obtained by biopsy show, in both cases, the loss of individual nerve fibers as an expression of a chronic axonal degeneration. The pathogenetic basis to be considered in these cases is presented.

Aged↗
PubMed1975

Oligodendroglial cell development in jimpy mice and controls. An electron-microscopic study in the optic nerve.

Glial development was studied in the optic nerve of 1- to 28-day-old Jimpy mice and controls. Abnormalities were found in oligodelopment and axons were not affected. These consisted in (a) Increased numbers of glioblastic cells containing lipids and increased occurrence of glial cell death in the premyelination stage; (b) Decreased numbers of maturing oligodendrocytes (i.e. young and active oligodendrocytes) in the period of early myelination; (c) An occurrence of abnormal oligodendroglial cells containing lipids and multimembranous tubes in the period of advanced myelination. The decreased number of maturing oligodendrocytes in the premyelination stage indicates that the lack of myelin in Jimpy mice may be secondary to a disturbance in the differentiation of the oligodendroglial cell line. The occurrence of abnormal, lipid-containing glioblasts and oligodendrocytes may be an expression of a defect in metabolism leading to an abnormality in the association of myelin proteins and myelin lipids.

Animals↗
PubMed1975

Progressive neural muscular atrophy in a case of phenylketonuria.

Clinical, neurophysiological and nerve-biopsy findings are described in a 13-1/2-year-old boy with classical phenylketonuria who developed progressive muscular atrophy. Clinical examination revealed atrophy of the calf muscles and pes varus. Tendon jerks were brisk in the upper extremities but were absent in the right leg and weak in the left leg. Nerve conduction velocities of the median and peroneal nerve were strongly reduced. Light- and electronmicroscopic investigation of sural nerve biopsy revealed axonal dystrophy and 'onion-bulb' formation of the Schwann cells. It is assumed that the combination of phenylketonuria and progressive muscular atrophy in this patient is an accidental occurrence.

Adolescent↗
PubMed1975

Prenatal metachromatic leukodystrophy.

In a family with a metachromatic leukodystrophy patient, two further pregnancies at risk were monitored by amnion cell culture. In one case, a normal baby was predicted and born. In the other case, a prenatal deficiency of arylsulfatase A was found. The diagnosis of metachromatic leukodystrophy was confirmed biochemically in various organs of the fetus by the deficiency of arylsulfatase A. The residual enzyme activity was shown to have an abnormal pH optimum and an increased heat stability. Ultrastructural studies revealed lipid storage in the myelinating nervous system and in the liver. For the interpretation of morphological results, it was indispensable to analyze an age-matched control fetus.

Arylsulfatases↗